Abstract

Conidia of Colletotrichum graminicola , the causal agent of corn anthracnose, begin to adhere to hydrophobic surfaces immediately after contact with the surface and hours before the onset of germination. Conidia rarely adhered to glass, a hydrophilic surface. The maximum percentage adhesion of ungerminated conidia was approx. 30–40% on polystyrene Petri dishes and 20–25% on dimethyldichlorosilane (DMS)-coated glass slides. The maximum adhesion on both surfaces was attained within 30 min of the time of contact. Thus, conidia appear to require hydrophobic surfaces for adhesion. The extracellular mucilage that is produced in association with conidia was shown to not be involved in adhesion. Adhesion was not influenced by conidium concentration but was influenced by conidium age. Exposure of conidia to different temperatures in adhesion assays delayed the ability of conidia to adhere. The respiration inhibitor, sodium azide and the transcription inhibitor, actinomycin D, had no effect on adhesion. In contrast, inhibitors of glycoprotein transport (brefeldin A) and protein synthesis (cycloheximide) reduced conidial adhesion by 30 and 50%, respectively. Treatment of conidia with pronase E prevented adhesion completely. If conidia were pre-treated with pronase E and then washed free of the enzyme, approx. 20 % of the conidial population recovered the ability to adhere. Conidia treated with Concanavalin A at a concentration of 1 mg ml −1 also failed to adhere. This effect was partially reversed by the haptens glucose and mannose. Together, these results suggest that glycoprotein synthesis is involved in the adhesion of ungerminated conidia.

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